logging in or signing up Bronchial asthma pathophysiology vijaysinh Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 1930 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: December 26, 2011 This Presentation is Public Favorites: 2 Presentation Description Asthama Comments Posting comment... Premium member Presentation Transcript PATHOPHYSIOLOGY OF ASTHMA Dr. V. K. Bhatlawande M.D. (Pediatrics) Consultant, Dr. Jagdale Mama Hospital, Barshi, Dist. Solapur.: PATHOPHYSIOLOGY OF ASTHMA Dr. V. K. Bhatlawande M.D. (Pediatrics) Consultant, Dr. Jagdale Mama Hospital, Barshi , Dist. Solapur .Asthma - Definition:: Asthma - Definition : characterized by - Increased responsiveness of the Tracheo-bronchial tree to multiplicity of stimuli.Asthma: Asthma R O A D + B H R Reversible Obstructive Airway Disease Bronchial Hyper - reactivityAsthma: Asthma 30 % children get wheezing illness in first three years. 10 - 20 % will develop asthma in later life. Sex – m : f = 2 : 1 upto adolescence. 1 : 1 in adultsRemission Occur in 50 % by 6 years. : Remission Occur in 50 % by 6 years. depends on- Severity of hyper-reactivity. Growth in diameter of bronchus. Physiologic hypertrophy of mucus glands regresses to normal. Bronchial cartilage and muscles development offer better support, prevent easy collapsePredisposing factors Allergens : Predisposing factors Allergens - Inhaled House dust, pollen, fungi, molds spores animal danders, cockroachesPredisposing factors Allergens: Predisposing factors Allergens Ingested - fish, nuts, strawberriesPredisposing factors - Allergen: Predisposing factors - Allergen Food Additives Tartrazine - yellow coloring agent Metabisulphite - used as preservatives Ajinomoto - Monosodium glutamatePredisposing factors – Allergen Occupational allergens : Predisposing factors – Allergen Occupational allergens Grain dust, wood dust, coffee, gum acacia Metal salts - Chromium, Nickle, Platinum Pharmaceuticals - Cimetidine, AntibioticsPredisposing factors Non-allergic: Predisposing factors Non-allergic Infections - viral (mainly) RSV, Adeno, Rhino - Bact - Chlamydia, Mycoplasma Exercise Environmental changes – temp, humidity Emotions - extreme joy, sorrowPredisposing factors Non-allergic: Predisposing factors Non-allergic Drugs - NSAID, Aspirin, Beta blockers, Methacholine R.O.C - environmental pollutants Ozone, NO2, SO2Genetic factors: Genetic factors Genotype + Environment = Phenotype Complex Genetic Disorder Heterogeneity of genes Incomplete penetration Variable expression Lack of mode of transmission Environmental influenceChromosome Regions Genes Implicated : Chromosome Regions Genes Implicated 11q, 13 - Regulation of IgE Signaling; Oxidative stress 5q 31-33 - * E'phil Mast cell Basophil - growth factor * Th 1 Polarization, Th 2 cytoclan; * Muscle Relaxation – B 2 agonist efficiency * IgE switching-differentiationChromosome Regions Genes Implicated : Chromosome Regions Genes Implicated 7q, 14q -> T-cell Receptor Genes Atopic Asthma - HLA DRB, 15; DQA 501; DQB,0301 Adren . receptor modifying - 12q; 13q; 16p;Nocturnal Asthma: Nocturnal Asthma Asthma attacks are more common at night WHY ?Nocturnal Asthma: Nocturnal Asthma Core temp decreases Sleep homeostat Lead to circadian changesNocturnal Asthma: Nocturnal Asthma FEV1 & P E F R are Max. - 4 pm / Min. - 4 am Vagal tone increases - Br. Narrowing Sympth tone - Peripheral venous bl. shifts to central compt. So engorgement of lungs. Br. reactivity increases to nonspecific stimuliCircadian hormonal changes: Circadian hormonal changes Hormonal binding decreases Tissue responsiveness decreases to Corticosreroids - Norepinephrine Reduced density of β adren. receptorsBronchoscopic studies at night: Bronchoscopic studies at night More inflammation at night Inflammatory cells eg Eosinophils, macrophages, neutrophils are more in broncho-alveolar lavage Degree of eosinophil infiltration coincides with decrease in airway caliberPathology: Pathology Bronchial smooth muscle contraction. Edema br. wall - Micro-vascular leakiness - Inflammatory cell reaction. Mucous gl. hypertrophy - excessive secretion. Basement membrane thickening. Luminal plug due to – Thick mucus - Desquamation of epithelium. - Entangled eosinophils.Pathology: PathologyAll these changes occur via Receptors What are receptors ?: All these changes occur via Receptors What are receptors ?Receptors – : Receptors – Gylco-proteins in the cell wall. They have rapid turnover as per need. In Asthma, receptors are malfunctioning due to presence of auto-antibodies, but they respond to agonist drugs.Receptors are influenced by: Receptors are influenced by Hormones (epinephrine, VIP, Substance P) Neuro transmitters 1- noradrenaline , muscarinic 1- Ach Mediators DrugsAUTONOMIC AIRWAY RECEPTORS : AUTONOMIC AIRWAY RECEPTORS Adrenergic Cholinergic (M) V.I.P. Substance P Br Musc Relaxation Contraction Submuc gla Secretion Secretion Mast Cell Secretion Secretion B V. Leakiness LeakinessMediators: Mediators Mediators causing – Br.constriction, Mucosal oedema Histamin - H 1 Leucotrine - B 4, C 4, D 4 Platelet Activating Factor - PAF Prostaglandin - D 2, Brady-KininMediator causing Bronco relaxation -: Mediator causing Bronco relaxation - prostaglandin E2PATHO-PHYSIOLOGY: PATHO-PHYSIOLOGY Antigen engulfed by macrophages Processed Presented on the surface to “T” cells Various subsets of cells formed. – T Helper, T suppressor, B helper, B suppressor, Cytokine secreting cells, N K cells Memory cellsPATHO-PHYSIOLOGY - : PATHO-PHYSIOLOGY - Macrophage processed Antigen Stimulates T cell TH2 cells in presence of IL 4, 13 Formation of IgE Attaches to receptors of Mast CellPATHO-PHYSIOLOGY -: PATHO-PHYSIOLOGY - Mast Cell Histamin Heparin Leucotrine B4, C4, Prostaglandin D2, F2 PAF Chemotactic factors Early attackEarly attack : Early attack Prevented by Mast cell stabilizing agents like chromolyn Treated by Beta agonistChemotactic factors: Chemotactic factors After 2- 8 hours – Eosinophils - major basic protein eosin. cationic protein more chemo-tactic factor. Destroy mucus memb. Slough – creola bodies Pevented - chromolyn, steroids T/t - steriodsPowerPoint Presentation: After 2 to 10 Days Basophil, monocyte mediators Attack may last for wks. No preventive drug T/t - Antiinflammatory, Bronchodialators Prone for complicationsPatho-physiology helps in treatment: Patho-physiology helps in treatment Mast cell stabilizer - chromo. Steroids LTE inhibitors – early, late phase Smooth mus. Relaxants Anti-inflammatory - in late phase Muco-lytic agents – N acetyl cystinCLINICAL FEATURES : CLINICAL FEATURES Stage 1 --- Cough variant asthma Bronchial obstruction interfers with gaseous exchange Hacking, Paroxysmal, Irrtative, Non-Productive Cough. T/t - responds to bronchodialatorsSTAGE 2 : STAGE 2 Mild to Moderate Asthma - Thick mucus secretion increases. - Desquamated epithelial slough & eosinophils get entangled. - Frothy gelatinous sputum. - Breathlessness.Stage 3 - very severe broncho – spasm.: Stage 3 - very severe broncho – spasm . - Respiratory rate > 40 in 5 to 15 yrs. > 50 - upto 5 yrs. - Accessary muscle in action - intercostal recession, nasal flaring, exp.grunting . head noddingStage 3 - very severe broncho – spasm.: Stage 3 - very severe broncho – spasm . - Pulse > 120 - 5 – 15 yrs, > 140 - upto 5 yrs. - PEFR < 50 % of predicted. - Talks in words. Cannot drink. - Altered consciousness - drowsy / agitated - Pulsus paradoxus > 40 mm hg - O2 saturation < 90 %, - Pa CO2 > 40 mm hg - Shallow irregular breathing, - sudden hypercapnea, - Chest may be silent. No ralesTreatment : Treatment Mild attack - agonist aerosol – salbutamol – MDI, Nebulisation for 5 min.Moderate To Severe Attack : Moderate To Severe Attack Oxygen - 4 – 6 Lit / Min. O2 Saturation >92 % Salbutamol - MDI - 2 Puffs / 5 Min. for upto 20 Puffs. Nebulisation- 0.15 mg/kg - 3 ml / 20 Min* 2 hrs. 3. Systemic Steroids - Hydrocortisone - 10 Mg/Kg Stat , Then 4 Mg/Kg/ 6 Hourl Methyl Prednisolone - 4 Mg/Kg single dose Oral Prednisolone - 1 to 2 Mg/Kg/ dose for 24 HoursModerate To Severe Attack: Moderate To Severe Attack 4. I.V. Fluids - 1.5 Volume of maintenance. If no response 5. Ipratropium bromide - nebulisation if no response 6. Aminophylline - 6 mg/kg slowly over 20 min. Then, IV drip 1 mg/kg/hour if no response 7. Volume cycled mechanical ventilation -Moderate To Severe Attack: Moderate To Severe Attack Adrenaline - 0.01 ml / kg / SC. May be given before nebulisation. Effect is equal to nebulisation. Side effects - pallor, palpitation, tremors, headache.Moderate To Severe Attack: Moderate To Severe Attack Assess after 1 hour for - Respiratory rate, Dyspnea, Rhonci, PEF, O2 saturation- Good Response: - Good Response No Breathlessness, Few rhonci, PEF > 70%. T/T - steroids + salbutamol for 5 days.- Moderate response - : - Moderate response - Breathlessness, Rhonci ++, PEF > 50% Salbutamol nebulisation / MDI every 4 hourly Steroids continued. Aminophylline drip is contd. Ipratropium bromide nebulisation every 4 hourlyPoor Response : Poor Response mechanical ventilation.Aerosol Therapy : Aerosol Therapy Liquid / solid particles < 5 microns suspended in gas. Depopsited in smaller airways. Dose required is very less. Reduces systemic side effects. Maximum effect seen after 10 minSympatho-mimetic Aerosols: Sympatho-mimetic Aerosols Salbutamol, Terbutalin, Salmeterol 0.01 to 0.03 ml / kg. (max. 1 ml) Steroids – Budesonide, Betamethasone, Beclomethasone Cromolyn - MDI - 20 Mg Cap. delivers 1 Mg Mucolytic - N-acetyl cysteine - 2ml / 2ml waterNewer drugs : Newer drugs Leucotrine receptor antagonist - Montalukast, Zafirlukast Used in BD dose for prevention & continuous treatment. Lucotrine synthesis preventing agent - zileutol IgE antibodies - rhumab – e25 Mast cell products antagonist - tryptase Chemokine antagonist - mcp 4 Cytokine antibodies Gene therapy - modulating TH2 receptors You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.